51 - Charcot Reconstruction Flashcards
1
Q
Deep thoughts with old man Greenhagen
A
- “In the last analysis, we see only what we are ready to see, what we have been taught to see. We eliminate and ignore everything that is not a part of our prejudices” Jean Martin Charcot
2
Q
Charcot neuropathy
A
- Non-infectious destruction of bone associated with neuropathy
- Initial recognition can be difficult
- Can be devastating
- Now common in diabetics with neuropathy
3
Q
A little history…
A
- Sir William Musgrave
o First to describe neuropathic joint 1703, called it “neuropathic arthritis” and noted that it was a complication of venereal disease (VD) - John Kearsley Mitchell
o Suggested a relationship between a spinal cord lesion(TB caries of the spine) and arthropathy of the foot and ankle, referenced by Charcot in his first papers - Silas Weir Mitchell
o Gunshot wounds during Civil War, nutrition of joints, spinal injury leads to rheumatic sx - Jean-Martin Charcot
o 1825-1893, one of most celebrated French physicians, transformed Salpetriere into world renowned institution
o Arthropathy associated with progressive locomotor ataxia (tabes dorsalis)
o Early findings published in 1868, referenced Mitchell and Mitchell - Virchow and Volkmann
- William Reily Jordan
4
Q
Pathophysiology
A
Pathophysiology
- 7th International Medical Congress – London, August 2-9, 1881
- “A gathering the like of which has never been witnessed before, and in all probability will never be paralleled in our day.” The Lancet
5
Q
Historical prospective
A
- 1936: Pathology linked to diabetes by WR Jordan
- 1955: Miller and Lichtman established the increasing frequency in diabetic patients
- 1966: Eichenholtz classified deformity based on radiographic progression KNOW THIS
6
Q
French theory = “Neurotrophic” theory
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- Central nervous system degeneration caused a neurogenic deficit in bone nutrition
- Known causes of neuropathic arthropathy at the time generally related to central injuries
- No trophic factors identified to support this theory
7
Q
German theory = “Neurotraumatic” theory
A
- Loss of protective sensation allows for repetitive microtrauma in the insensate limb
- Normal fracture healing does not occur
- Volkman and Virchow argued that neuroarthropathy was merely “traumatic arthritis”
- Fails to explain development in paralyzed patients unable to ambulate
8
Q
Neurovascular theory – TODAY’S THEORY
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- Increased blood flow in region of destruction – they’re bright red, so we know there is blood
- Sympathetic failure causes a hyper-vascular reflex and a state of overactive bone resorption
- Bone scans show increased uptake in Charcot arthropathy
- Due to sympathetic denervation or local inflammatory process?
9
Q
The common denominator of disorders which cause neuropathic arthropathy is:
A
“The absence or decrease in pain sensation in the presence of uninterrupted physical activity” o Tabes dorsalis or syringomyelia o Congenital insensitivity to pain o Spinal Cord Injury or peripheral Nerve Inj. o Idiopathic neuropathy o Diabetes o Leprosy o Myelomenigocele or Spina Bifida o Chronic Alcoholism o Transplant patients or chemotherapy
10
Q
REMEMBER: Charcot is…
A
REMEMBER: Charcot is NEURO-ARTHROPATHY ***
11
Q
Unifying theory
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- Best understanding of the etiology of neuropathic arthropathy at this point is multifactorial
- Balance between RANKL (receptor activator of nuclear factor kappa beta ligand) and osteoprotegerin (OPG)
- RANKL activates RANK, osteoclasts, etc. in order to cause bone destruction
- OPG has opposite effect – it stops RANKL form binding and therefore prevents osteoclasts from becoming activated and resorbing bone
- Vascular calcification in DM occurs by same pathway (intima-MEDIA-adventitia) – If you see vascular calcification, be suspicious
12
Q
RANKL/OPG signaling pathology
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- RANKL binds to RANK, inducing a signaling cascade leading to differentiation of osteoclast precursor cells and stimulating the activity of mature osteoclasts
- Functions as a decoy receptor for RANKL, and is thus an inhibitor of osteoclastogenesis
13
Q
Amount of bone resorption depends on the balance of RANKL and OPG
A
- If RANKL and OPG are present in equal amounts, bone is maintaining itself
- If RANKL is at a higher concentration, more bone resorption occurs
- If OPG is at a higher concentration, less bone resorption occurs
14
Q
BMD and patterns of Charcot’s Arthropathy
A
- Patient suffering from Charcot have altered bone mineral density (BMD)
- Herbst et al, 2004 showed that patients with normal BMD tend to have dislocations due to trauma and patients with diminished BMD tend to have fractures due to trauma
- Greenhagen et al, 2011 showed that BMD does not seem to recover after a Charcot event
15
Q
Typical patient
A
- 55-60 yrs. old (mean 57), mean years as a diabetic is 15 yrs. w/ 80% having it for at least 10 yrs.
- Prevalence varies with ranges from 0.03% to 7.5%, so a good ballpark number is 1%
- **Bilateral involvement in 9-35% ** because when you treat one side, it typically involves off-loading, leading to overuse to the other side and eventually Charcot
- The longer you have diabetes, the worse your Charcot because the worse your neuropathy
- A diabetic with neuropathy is classified as a “complicated diabetic”
16
Q
Epidemiology
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- Sinha, et al, in one of the first large studies on diabetics with Charcot, reported that 1 in 680 diabetics had Charcot (n = 68,000)
- 10 year Danish study (n = 4000) found an annual incidence of initial Charcot attack of 0.3%
- Lavery et al, 2003 (n = 1666 diabetics) found a much higher in US (11-6%)
- True prevalence unknown – could be as high as 25% when considering wrong diagnoses
17
Q
Diagnosis of Charcot - Three aspects to consider
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o History
o Physical Exam
o Radiographic Interpretation
18
Q
Diagnosis history
A
- Hot, Swollen Foot
- +/- Trauma
- Just because they don’t remember trauma doesn’t mean they didn’t have it – 55-75% do not remember any trauma
- Trauma is not limited to sprains and strain – Joint infections and surgical trauma can induce this
- Mild/ moderate pain (if you can’t feel anything but you can feel pain – WARNING SIGN)
- No previous ulcerations and no systemic signs of infection
19
Q
Diagnosis physical exam
A
- Swollen, (deformed?) Foot
- Warmth
- Erythema
- Joint effusion
- Neuropathy
- +/- Ulcerations
- Contralateral foot
- Elevation test – with inflammation/venous stasis, patient will demonstrate dependent rubor with elevation pallor
20
Q
Typical acute presentation
A
- So, the typical acute presentation of a Charcot foot is a red, hot, swollen foot
- Typically this is painless or only mildly painful unilateral swelling of extremity
- The Acute presentation can mimic cellulitis, gout, osteomyelitis and even DVT
- Plain films may appear normal initially
- Physical exam may reveal joint laxity w/ crepitus, decreased DTRs, vibration, and proprioception
- Patient may have bounding pulses, calor, rubor, tumor, anhidrosis +/- xerosis, cutaneous ulcer
- In the chronic Charcot you may see a Rocker bottom foot with plantar ulcerations
21
Q
Natural history
A
- Advanced Glycosylation (pull of triceps, intrinsic atrophy, alters mechanical bone properties)
- Midfoot Collapses and Reversal of Arch (“rockerbottom” deformity)
- Tarsal prominence leads to Increased Plantar Pressure
22
Q
Diagnosis – X-ray
A
- EARLIEST sign is bone resorption and soft tissue swelling, before architecture is altered
- Bony destruction, Fracture, Subluxation and Dislocation may also occur
- No wound = no osteo (hematogenous osteo is typically in kids due to high blood turbulence at growth plates, so unless there is or has been an open wound, it’s not osteo)
23
Q
Brodsky Anatomic Classification
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Really important because the majority of research is ortho
- Type 1
- Type 2
- Type 3a/3b
24
Q
Brodsky Anatomic Classification - Type 1
A
o Tarsometarsal and naviculocuneiform jts - MIDFOOT
o MOST COMMON (60%) and most stable
25
Q
Brodsky Anatomic Classification - Type 2
A
o Transverse tarsal and subtalar joints
o Second most common (35 %)
o Hindfoot instability leading to ulceration, typically over the talar head
26
Q
Brodsky Anatomic Classification - Type 3a/3b
A
3a = ankle 3b = calcaneus
o 5% of Charcot but MOST UNSTABLE
o Frequently requires surgery, high risk of major amputation (BKA, AKA)
o VERY UNSTABLE
27
Q
Sanders and Frykberg Classification
A
Main difference is “Pattern I” which focuses on forefoot Charcot
- Pattern I
- Pattern II
- Pattern III
- Pattern IV
- Pattern V
28
Q
Sanders and Frykberg Classification - Pattern I
A
Pattern I: Forefoot (15%)
o IPJs and phalanges
o MPJs and metatarsals
